title: Pretreatment cognitive deficits and treatment effects on attention in childhood absence epilepsy.
abstract: OBJECTIVE
  To determine the neurocognitive deficits associated with newly diagnosed untreated childhood absence epilepsy (CAE), develop a model describing the factorial structure of items measuring academic achievement and 3 neuropsychological constructs, and determine short-term differential neuropsychological effects on attention among ethosuximide, valproic acid, and lamotrigine.
  
  
  METHODS
  Subjects with newly diagnosed CAE entering a double-blind, randomized controlled clinical trial had neuropsychological testing including assessments of general intellectual functioning, attention, memory, executive function, and achievement. Attention was reassessed at the week 16-20 visit.
  
  
  RESULTS
  At study entry, 36% of the cohort exhibited attention deficits despite otherwise intact neurocognitive functioning. Structural equation modeling of baseline neuropsychological data revealed a direct sequential effect among attention, memory, executive function, and academic achievement. At the week 16-20 visit, attention deficits persisted even if seizure freedom was attained. More subjects receiving valproic acid (49%) had attention deficits than subjects receiving ethosuximide (32%) or lamotrigine (24%) (p = 0.0006). Parental assessment did not reliably detect attention deficits before or after treatment (p < 0.0001).
  
  
  CONCLUSIONS
  Children with CAE have a high rate of pretreatment attentional deficits that persist despite seizure freedom. Rates are disproportionately higher for valproic acid treatment compared with ethosuximide or lamotrigine. Parents do not recognize these attentional deficits. These deficits present a threat to academic achievement. Vigilant cognitive and behavioral assessment of these children is warranted.
  
  
  METHODS
  This study provides Class I evidence that valproic acid is associated with more significant attentional dysfunction than ethosuximide or lamotrigine in children with newly diagnosed CAE.
authors.affiliation: From the Montefiore Medical Center (D.M., S.S., R.C.S., E.F.W.), Albert Einstein College of Medicine, New York; Children's National Medical Center (A.C., J.W.), Washington, DC; National Institute of Neurological Disorders and Stroke (D.G.H.), Bethesda, MD; and Cincinnati Children's Hospital Medical Center, and University of Cincinnati College of Medicine (P.C., T.A.G.), OH.
authors.forename: David
authors.initials: D
authors.lastname: Masur
authors.forename: Shlomo
authors.initials: S
authors.lastname: Shinnar
authors.forename: Avital
authors.initials: A
authors.lastname: Cnaan
authors.forename: Ruth C
authors.initials: RC
authors.lastname: Shinnar
authors.forename: Peggy
authors.initials: P
authors.lastname: Clark
authors.forename: Jichuan
authors.initials: J
authors.lastname: Wang
authors.forename: Erica F
authors.initials: EF
authors.lastname: Weiss
authors.forename: Deborah G
authors.initials: DG
authors.lastname: Hirtz
authors.forename: Tracy A
authors.initials: TA
authors.lastname: Glauser
mesh_terms: D000293:Adolescent; D000704:Analysis of Variance; D000927:Anticonvulsants / Q000627:therapeutic use*; D001289:Attention Deficit Disorder with Hyperactivity / Q000188:drug therapy* / Q000209:etiology*; D002648:Child; D002675:Child, Preschool; D003072:Cognition Disorders / Q000209:etiology*; D015331:Cohort Studies; D004311:Double-Blind Method; D004522:Educational Status; D004569:Electroencephalography; D004832:Epilepsy, Absence / Q000150:complications*; D056344:Executive Function; D005260:Female; D006801:Humans; D008297:Male; D009483:Neuropsychological Tests; D016896:Treatment Outcome
chemical_list: D000927:Anticonvulsants